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quinidine/inflammation
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Evaluation of para-Aminosalicylic Acid as a Substrate of Multiple Solute Carrier Uptake Transporters and Possible Drug Interactions with Nonsteroidal Anti-inflammatory Drugs In Vitro.
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para-Aminosalicylic acid (PAS) is a second-line antituberculosis drug that has been used to treat multidrug-resistant and extensively drug-resistant tuberculosis for more than 60 years. Renal secretion and glomerular filtration are the major pathways for the elimination of PAS. We comprehensively
Pharmacokinetics of baicalin in rats and its interactions with cyclosporin A, quinidine and SKF-525A: a microdialysis study.
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Baicalin, a flavone glucuronide derived mainly from the root of Scutellaria baicalensis, has been used in traditional Chinese medicine as an anti-inflammatory and anti-viral agent. To explore whether the disposition of baicalin is related to multidrug resistance P-glycoprotein (P-gp), baicalin (3,
Toxic epidermal necrolysis associated with quinidine administration.
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Toxic epidermal necrolysis (TEN) is a rare, life threatening, drug induced cutaneous reaction first reported by Lyell in 1956. He named the condition TEN to distinguish it from staphylococcal scalded skin syndrome. It is characterized by a separation of the epidermis and dermis with subsequent
Ultraviolet B irradiation inhibits the induction of photoallergy to systemically administered quinidine in the mouse.
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In albino mice photosensitized to quinidine, 100 mg/kg by intraperitoneal injection, pretreatment of the induction area with ultraviolet B (UVB) on 3 consecutive days was shown to significantly reduce the inflammatory response when the mice were challenged at a distant site 1 week later. Mice
Differences in pharmacokinetics and hepatobiliary transport of a novel anti-inflammatory agent between normal and adjuvant arthritis rats.
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1. The pharmacokinetics, particularly the hepatobiliary transport of T-5557 ((3-methyl-2-oxo-piperadin-3-yl)-acetic acid N'-(3-thieophen-2-yl-8-methoxy-quinazolin-1-yl)-hydrazide), a novel anti-inflammatory agent, has been examined in normal and adjuvant arthritis (AA) rats. 2. Following oral
Chloroquine, quinine, procaine, quinidine and clomipramine are prostaglandin agonists and antagonists.
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Chloroquine, quinine, procaine, quinidine and clomipramine behave as prostaglandin (PG) antagonists in a rat mesenteric vascular bed preparation. The ID50 concentrations were within the range of therapeutically effective human plasma levels in each case. Antagonism to PGE2 was studied in detail and
Prevention of ischaemia-induced biochemical changes by curcumin & quinidine in the cat heart.
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Effect of myocardial ischaemia on the bioantioxidants levels in the cat heart was evaluated. In addition, effect of curcumin, an anti-inflammatory and anti-thrombotic drug, and quinidine, a standard antiarrhythmic drug, was also studied in the cat. Myocardial ischaemia was induced by the ligation of
The metabolism of diclofenac--enzymology and toxicology perspectives.
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Diclofenac is a nonsteroidal anti-inflammatory drug bearing a carboxylic acid functional group. As a result, the metabolism of diclofenac in humans partitions between acyl glucuronidation and phenyl hydroxylation, with the former reaction catalyzed primarily by uridine 5'-diphosphoglucuronosyl
Sudden death after catheter-induced atrioventricular junctional ablation.
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Atrioventricular (AV) junctional ablation was performed in a 59-year-old woman with recurrent atrial fibrillation refractory to treatment with digoxin, beta-blockers, verapamil, quinidine, procainamide, and amiodarone. She received two shocks of 500 J which produced complete AV block. After six
Involvement of gap junction channels in the pathophysiology of migraine with aura.
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Migraine is a common, recurrent, and disabling primary headache disorder with a genetic component which affects up to 20% of the population. One third of all patients with migraine experiences aura, a focal neurological disturbance that manifests itself as visual, sensitive or motor symptoms
Drug interactions with diuretics.
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Interactions between diuretics and other substances may have beneficial or adverse consequences. Co-prescription of diuretics with antihypertensive agents, potassium, magnesium or acid salts, probenecid, quinidine, anticoagulants, lithium, cardiac glycosides or other diuretics can result in both
Repurposing psychiatric medicines to target activated microglia in anxious mild cognitive impairment and early Parkinson's disease.
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Anxiety is common in the Mild Cognitive Impairment (MCI) stage of Alzheimer's disease (AD) and the pre-motor stages of Parkinson's disease (PD). A concomitant and possible cause of this anxiety is microglial activation, also considered a key promoter of neurodegeneration in MCI and early PD via
[Early cardiotoxicity of Hydroxychloroquine].
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BACKGROUND
Hydroxychloroquine (HCQ) is most frequently used in the treatment of systemic inflammatory diseases. Cardiac complications of anti-malarial drugs are uncommon, and most of the time are the result of a long-term exposition. In this case, cardiotoxicity is the consequence of the lysosomal
Benzydamine N-oxygenation as an index for flavin-containing monooxygenase activity and benzydamine N-demethylation by cytochrome P450 enzymes in liver microsomes from rats, dogs, monkeys, and humans.
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Benzydamine is an anti-inflammatory drug that undergoes flavin-containing monooxygenase (FMO)-dependent metabolism to benzydamine N-oxide; however, benzydamine N-demethylation is also catalyzed by liver microsomes. In this study, benzydamine N-oxygenation and N-demethylation mediated by liver
Comparative inhibitory effects of different compounds on rat oatpl (slc21a1)- and Oatp2 (Slc21a5)-mediated transport.
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OBJECTIVE
The purpose of the present study is to examine the selectivity of various inhibitors towards the rat organic anion transporting polypeptides 1 (Oatp1: gene symbol Slc21a1) and 2 (Oatp2: Slc21a5).
METHODS
The inhibitory effects of 20 compounds on the Oatpl-mediated transport of estradiol
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